The Experts below are selected from a list of 11565 Experts worldwide ranked by ideXlab platform
Sadao Kamidono - One of the best experts on this subject based on the ideXlab platform.
-
stress protein grp78 prevents apoptosis induced by Calcium Ionophore ionomycin but not by glycosylation inhibitor tunicamycin in human prostate cancer cells
Journal of Cellular Biochemistry, 2000Co-Authors: Hideaki Miyake, Isao Hara, Soichi Arakawa, Sadao KamidonoAbstract:GRP78 induction has recently been shown to play a critical role in maintaining cell viability against several kinds of stress, including depletion of endoplasmic reticulum Ca(2+) and accumulation of unglycosylated proteins, under specific experimental conditions. However, the functional significance of GRP78 induction after stressful treatment has not been well defined. This article characterizes the different biological features associated with GRP78 induction by two kinds of stress agents, Calcium Ionophore, ionomycin (IM), and glycosylation inhibitor, tunicamycin (TM), focusing on the association with apoptosis in human prostate cancer cells. Both IM and TM treatment resulted in marked induction of GRP78 transcription in androgen-dependent prostate cancer LNCaP cells maintained in medium without androgen, but not in medium containing androgen, as measured by Northern blotting and nuclear run-off assays. After pretreatment with tumor necrosis factor-alpha, which has potent cytotoxic effects on LNCaP cells, both IM and TM could induce substantial increases in GRP78 transcription in LNCaP cells, even in medium containing androgen. Under both experimental conditions described, DNA fragmentation assays showed a direct correlation between the onset of apoptosis in LNCaP cells after IM treatment and the initiation of GRP78 transcript induction, while induction of GRP78 expression preceded TM-induced apoptosis. To elucidate the functional differences of GRP78 induction by IM and TM, an antisense oligodeoxynucleotide (ODN) targeted against the grp78 gene was designed to reduce GRP78 expression in a sequence-specific and dose-dependent manner. Antisense GRP78 ODN treatment substantially enhanced apoptosis of LNCaP cells induced by IM compared with mismatch control ODN treatment, whereas no marked differences were observed in apoptotic features induced by TM with antisense GRP78 and mismatch control ODN treatment. Studies of additional androgen-independent prostate cancer PC3 cells also demonstrated a correlation between GRP78 induction and resistance to apoptosis after IM treatment, but not after TM treatment. These findings suggest that there are at least two GRP78 signaling pathways, which play different roles in resistance against stress-induced apoptosis.
-
stress protein grp78 prevents apoptosis induced by Calcium Ionophore ionomycin but not by glycosylation inhibitor tunicamycin in human prostate cancer cells
Journal of Cellular Biochemistry, 2000Co-Authors: Hideaki Miyake, Isao Hara, Soichi Arakawa, Sadao KamidonoAbstract:GRP78 induction has recently been shown to play a critical role in maintaining cell viability against several kinds of stress, including depletion of endoplasmic reticulum Ca2+ and accumulation of unglycosylated proteins, under specific experimental conditions. However, the functional significance of GRP78 induction after stressful treatment has not been well defined. This article characterizes the different biological features associated with GRP78 induction by two kinds of stress agents, Calcium Ionophore, ionomycin (IM), and glycosylation inhibitor, tunicamycin (TM), focusing on the association with apoptosis in human prostate cancer cells. Both IM and TM treatment resulted in marked induction of GRP78 transcription in androgen-dependent prostate cancer LNCaP cells maintained in medium without androgen, but not in medium containing androgen, as measured by Northern blotting and nuclear run-off assays. After pretreatment with tumor necrosis factor-α, which has potent cytotoxic effects on LNCaP cells, both IM and TM could induce substantial increases in GRP78 transcription in LNCaP cells, even in medium containing androgen. Under both experimental conditions described, DNA fragmentation assays showed a direct correlation between the onset of apoptosis in LNCaP cells after IM treatment and the initiation of GRP78 transcript induction, while induction of GRP78 expression preceded TM-induced apoptosis. To elucidate the functional differences of GRP78 induction by IM and TM, an antisense oligodeoxynucleotide (ODN) targeted against the grp78 gene was designed to reduce GRP78 expression in a sequence-specific and dose-dependent manner. Antisense GRP78 ODN treatment substantially enhanced apoptosis of LNCaP cells induced by IM compared with mismatch control ODN treatment, whereas no marked differences were observed in apoptotic features induced by TM with antisense GRP78 and mismatch control ODN treatment. Studies of additional androgen-independent prostate cancer PC3 cells also demonstrated a correlation between GRP78 induction and resistance to apoptosis after IM treatment, but not after TM treatment. These findings suggest that there are at least two GRP78 signaling pathways, which play different roles in resistance against stress-induced apoptosis. J. Cell. Biochem. 77:396–408, 2000. © 2000 Wiley-Liss, Inc.
-
Calcium Ionophore ionomycin inhibits growth of human bladder cancer cells both in vitro and in vivo with alteration of bcl 2 and bax expression levels
The Journal of Urology, 1999Co-Authors: Hideaki Miyake, Isao Hara, Kazuki Yamanaka, Soichi Arakawa, Sadao KamidonoAbstract:AbstractPurpose: The objective of this study was to characterize the antiproliferative effects of the Calcium Ionophore, ionomycin on the human bladder cancer cell line HT1376 both in vitro and in ...
Mario Sousa - One of the best experts on this subject based on the ideXlab platform.
-
more than 90 fertilization rates after intracytoplasmic sperm injection and artificial induction of oocyte activation with Calcium Ionophore
Fertility and Sterility, 1995Co-Authors: Jan Tesarik, Mario SousaAbstract:Objective To examine whether fertilization rates after intracytoplasmic sperm injection can be increased by artificial oocyte activation. Design Oocytes that failed to fertilize spontaneously by 24hours after intracytoplasmic sperm injection were treated either with Calcium Ionophore to induce activation or with solvent only to serve as control. The ability of Ionophore-treated and control oocytes to achieve delayed fertilization was compared. Setting Private hospital and public research center. Patients Infertile couples treated by intracytoplasmic sperm injection. Interventions Intracytoplasmic sperm injection. Main Outcome Measures Fertilization and cleavage rates. Results The mean rate of spontaneous fertilization after intracytoplasmic sperm injection was 32%, but 88% of the oocytes that failed to fertilize spontaneously did so after subsequent exposure to Calcium Ionophore. Most of these oocytes underwent at least one apparently normal cleavage division. In contrast, delayed fertilization of oocytes not treated with Ionophore was an exceptional finding. If only oocytes remaining intact after intracytoplasmic sperm injection are taken into account, the mean global fertilization rate of Ionophore-enhanced intracytoplasmic sperm injection was 91%. Conclusions These results show that the failure of oocyte activation is the main cause of fertilization failure after intracytoplasmic sperm injection. If an appropriate, clinically applicable treatment is found to overcome this problem, intracytoplasmic sperm injection can be expected to yield fertilization rates far exceeding those of standard IVF with normal spermatozoa.
Hideaki Miyake - One of the best experts on this subject based on the ideXlab platform.
-
stress protein grp78 prevents apoptosis induced by Calcium Ionophore ionomycin but not by glycosylation inhibitor tunicamycin in human prostate cancer cells
Journal of Cellular Biochemistry, 2000Co-Authors: Hideaki Miyake, Isao Hara, Soichi Arakawa, Sadao KamidonoAbstract:GRP78 induction has recently been shown to play a critical role in maintaining cell viability against several kinds of stress, including depletion of endoplasmic reticulum Ca(2+) and accumulation of unglycosylated proteins, under specific experimental conditions. However, the functional significance of GRP78 induction after stressful treatment has not been well defined. This article characterizes the different biological features associated with GRP78 induction by two kinds of stress agents, Calcium Ionophore, ionomycin (IM), and glycosylation inhibitor, tunicamycin (TM), focusing on the association with apoptosis in human prostate cancer cells. Both IM and TM treatment resulted in marked induction of GRP78 transcription in androgen-dependent prostate cancer LNCaP cells maintained in medium without androgen, but not in medium containing androgen, as measured by Northern blotting and nuclear run-off assays. After pretreatment with tumor necrosis factor-alpha, which has potent cytotoxic effects on LNCaP cells, both IM and TM could induce substantial increases in GRP78 transcription in LNCaP cells, even in medium containing androgen. Under both experimental conditions described, DNA fragmentation assays showed a direct correlation between the onset of apoptosis in LNCaP cells after IM treatment and the initiation of GRP78 transcript induction, while induction of GRP78 expression preceded TM-induced apoptosis. To elucidate the functional differences of GRP78 induction by IM and TM, an antisense oligodeoxynucleotide (ODN) targeted against the grp78 gene was designed to reduce GRP78 expression in a sequence-specific and dose-dependent manner. Antisense GRP78 ODN treatment substantially enhanced apoptosis of LNCaP cells induced by IM compared with mismatch control ODN treatment, whereas no marked differences were observed in apoptotic features induced by TM with antisense GRP78 and mismatch control ODN treatment. Studies of additional androgen-independent prostate cancer PC3 cells also demonstrated a correlation between GRP78 induction and resistance to apoptosis after IM treatment, but not after TM treatment. These findings suggest that there are at least two GRP78 signaling pathways, which play different roles in resistance against stress-induced apoptosis.
-
stress protein grp78 prevents apoptosis induced by Calcium Ionophore ionomycin but not by glycosylation inhibitor tunicamycin in human prostate cancer cells
Journal of Cellular Biochemistry, 2000Co-Authors: Hideaki Miyake, Isao Hara, Soichi Arakawa, Sadao KamidonoAbstract:GRP78 induction has recently been shown to play a critical role in maintaining cell viability against several kinds of stress, including depletion of endoplasmic reticulum Ca2+ and accumulation of unglycosylated proteins, under specific experimental conditions. However, the functional significance of GRP78 induction after stressful treatment has not been well defined. This article characterizes the different biological features associated with GRP78 induction by two kinds of stress agents, Calcium Ionophore, ionomycin (IM), and glycosylation inhibitor, tunicamycin (TM), focusing on the association with apoptosis in human prostate cancer cells. Both IM and TM treatment resulted in marked induction of GRP78 transcription in androgen-dependent prostate cancer LNCaP cells maintained in medium without androgen, but not in medium containing androgen, as measured by Northern blotting and nuclear run-off assays. After pretreatment with tumor necrosis factor-α, which has potent cytotoxic effects on LNCaP cells, both IM and TM could induce substantial increases in GRP78 transcription in LNCaP cells, even in medium containing androgen. Under both experimental conditions described, DNA fragmentation assays showed a direct correlation between the onset of apoptosis in LNCaP cells after IM treatment and the initiation of GRP78 transcript induction, while induction of GRP78 expression preceded TM-induced apoptosis. To elucidate the functional differences of GRP78 induction by IM and TM, an antisense oligodeoxynucleotide (ODN) targeted against the grp78 gene was designed to reduce GRP78 expression in a sequence-specific and dose-dependent manner. Antisense GRP78 ODN treatment substantially enhanced apoptosis of LNCaP cells induced by IM compared with mismatch control ODN treatment, whereas no marked differences were observed in apoptotic features induced by TM with antisense GRP78 and mismatch control ODN treatment. Studies of additional androgen-independent prostate cancer PC3 cells also demonstrated a correlation between GRP78 induction and resistance to apoptosis after IM treatment, but not after TM treatment. These findings suggest that there are at least two GRP78 signaling pathways, which play different roles in resistance against stress-induced apoptosis. J. Cell. Biochem. 77:396–408, 2000. © 2000 Wiley-Liss, Inc.
-
Calcium Ionophore ionomycin inhibits growth of human bladder cancer cells both in vitro and in vivo with alteration of bcl 2 and bax expression levels
The Journal of Urology, 1999Co-Authors: Hideaki Miyake, Isao Hara, Kazuki Yamanaka, Soichi Arakawa, Sadao KamidonoAbstract:AbstractPurpose: The objective of this study was to characterize the antiproliferative effects of the Calcium Ionophore, ionomycin on the human bladder cancer cell line HT1376 both in vitro and in ...
Soichi Arakawa - One of the best experts on this subject based on the ideXlab platform.
-
stress protein grp78 prevents apoptosis induced by Calcium Ionophore ionomycin but not by glycosylation inhibitor tunicamycin in human prostate cancer cells
Journal of Cellular Biochemistry, 2000Co-Authors: Hideaki Miyake, Isao Hara, Soichi Arakawa, Sadao KamidonoAbstract:GRP78 induction has recently been shown to play a critical role in maintaining cell viability against several kinds of stress, including depletion of endoplasmic reticulum Ca(2+) and accumulation of unglycosylated proteins, under specific experimental conditions. However, the functional significance of GRP78 induction after stressful treatment has not been well defined. This article characterizes the different biological features associated with GRP78 induction by two kinds of stress agents, Calcium Ionophore, ionomycin (IM), and glycosylation inhibitor, tunicamycin (TM), focusing on the association with apoptosis in human prostate cancer cells. Both IM and TM treatment resulted in marked induction of GRP78 transcription in androgen-dependent prostate cancer LNCaP cells maintained in medium without androgen, but not in medium containing androgen, as measured by Northern blotting and nuclear run-off assays. After pretreatment with tumor necrosis factor-alpha, which has potent cytotoxic effects on LNCaP cells, both IM and TM could induce substantial increases in GRP78 transcription in LNCaP cells, even in medium containing androgen. Under both experimental conditions described, DNA fragmentation assays showed a direct correlation between the onset of apoptosis in LNCaP cells after IM treatment and the initiation of GRP78 transcript induction, while induction of GRP78 expression preceded TM-induced apoptosis. To elucidate the functional differences of GRP78 induction by IM and TM, an antisense oligodeoxynucleotide (ODN) targeted against the grp78 gene was designed to reduce GRP78 expression in a sequence-specific and dose-dependent manner. Antisense GRP78 ODN treatment substantially enhanced apoptosis of LNCaP cells induced by IM compared with mismatch control ODN treatment, whereas no marked differences were observed in apoptotic features induced by TM with antisense GRP78 and mismatch control ODN treatment. Studies of additional androgen-independent prostate cancer PC3 cells also demonstrated a correlation between GRP78 induction and resistance to apoptosis after IM treatment, but not after TM treatment. These findings suggest that there are at least two GRP78 signaling pathways, which play different roles in resistance against stress-induced apoptosis.
-
stress protein grp78 prevents apoptosis induced by Calcium Ionophore ionomycin but not by glycosylation inhibitor tunicamycin in human prostate cancer cells
Journal of Cellular Biochemistry, 2000Co-Authors: Hideaki Miyake, Isao Hara, Soichi Arakawa, Sadao KamidonoAbstract:GRP78 induction has recently been shown to play a critical role in maintaining cell viability against several kinds of stress, including depletion of endoplasmic reticulum Ca2+ and accumulation of unglycosylated proteins, under specific experimental conditions. However, the functional significance of GRP78 induction after stressful treatment has not been well defined. This article characterizes the different biological features associated with GRP78 induction by two kinds of stress agents, Calcium Ionophore, ionomycin (IM), and glycosylation inhibitor, tunicamycin (TM), focusing on the association with apoptosis in human prostate cancer cells. Both IM and TM treatment resulted in marked induction of GRP78 transcription in androgen-dependent prostate cancer LNCaP cells maintained in medium without androgen, but not in medium containing androgen, as measured by Northern blotting and nuclear run-off assays. After pretreatment with tumor necrosis factor-α, which has potent cytotoxic effects on LNCaP cells, both IM and TM could induce substantial increases in GRP78 transcription in LNCaP cells, even in medium containing androgen. Under both experimental conditions described, DNA fragmentation assays showed a direct correlation between the onset of apoptosis in LNCaP cells after IM treatment and the initiation of GRP78 transcript induction, while induction of GRP78 expression preceded TM-induced apoptosis. To elucidate the functional differences of GRP78 induction by IM and TM, an antisense oligodeoxynucleotide (ODN) targeted against the grp78 gene was designed to reduce GRP78 expression in a sequence-specific and dose-dependent manner. Antisense GRP78 ODN treatment substantially enhanced apoptosis of LNCaP cells induced by IM compared with mismatch control ODN treatment, whereas no marked differences were observed in apoptotic features induced by TM with antisense GRP78 and mismatch control ODN treatment. Studies of additional androgen-independent prostate cancer PC3 cells also demonstrated a correlation between GRP78 induction and resistance to apoptosis after IM treatment, but not after TM treatment. These findings suggest that there are at least two GRP78 signaling pathways, which play different roles in resistance against stress-induced apoptosis. J. Cell. Biochem. 77:396–408, 2000. © 2000 Wiley-Liss, Inc.
-
Calcium Ionophore ionomycin inhibits growth of human bladder cancer cells both in vitro and in vivo with alteration of bcl 2 and bax expression levels
The Journal of Urology, 1999Co-Authors: Hideaki Miyake, Isao Hara, Kazuki Yamanaka, Soichi Arakawa, Sadao KamidonoAbstract:AbstractPurpose: The objective of this study was to characterize the antiproliferative effects of the Calcium Ionophore, ionomycin on the human bladder cancer cell line HT1376 both in vitro and in ...
Isao Hara - One of the best experts on this subject based on the ideXlab platform.
-
stress protein grp78 prevents apoptosis induced by Calcium Ionophore ionomycin but not by glycosylation inhibitor tunicamycin in human prostate cancer cells
Journal of Cellular Biochemistry, 2000Co-Authors: Hideaki Miyake, Isao Hara, Soichi Arakawa, Sadao KamidonoAbstract:GRP78 induction has recently been shown to play a critical role in maintaining cell viability against several kinds of stress, including depletion of endoplasmic reticulum Ca(2+) and accumulation of unglycosylated proteins, under specific experimental conditions. However, the functional significance of GRP78 induction after stressful treatment has not been well defined. This article characterizes the different biological features associated with GRP78 induction by two kinds of stress agents, Calcium Ionophore, ionomycin (IM), and glycosylation inhibitor, tunicamycin (TM), focusing on the association with apoptosis in human prostate cancer cells. Both IM and TM treatment resulted in marked induction of GRP78 transcription in androgen-dependent prostate cancer LNCaP cells maintained in medium without androgen, but not in medium containing androgen, as measured by Northern blotting and nuclear run-off assays. After pretreatment with tumor necrosis factor-alpha, which has potent cytotoxic effects on LNCaP cells, both IM and TM could induce substantial increases in GRP78 transcription in LNCaP cells, even in medium containing androgen. Under both experimental conditions described, DNA fragmentation assays showed a direct correlation between the onset of apoptosis in LNCaP cells after IM treatment and the initiation of GRP78 transcript induction, while induction of GRP78 expression preceded TM-induced apoptosis. To elucidate the functional differences of GRP78 induction by IM and TM, an antisense oligodeoxynucleotide (ODN) targeted against the grp78 gene was designed to reduce GRP78 expression in a sequence-specific and dose-dependent manner. Antisense GRP78 ODN treatment substantially enhanced apoptosis of LNCaP cells induced by IM compared with mismatch control ODN treatment, whereas no marked differences were observed in apoptotic features induced by TM with antisense GRP78 and mismatch control ODN treatment. Studies of additional androgen-independent prostate cancer PC3 cells also demonstrated a correlation between GRP78 induction and resistance to apoptosis after IM treatment, but not after TM treatment. These findings suggest that there are at least two GRP78 signaling pathways, which play different roles in resistance against stress-induced apoptosis.
-
stress protein grp78 prevents apoptosis induced by Calcium Ionophore ionomycin but not by glycosylation inhibitor tunicamycin in human prostate cancer cells
Journal of Cellular Biochemistry, 2000Co-Authors: Hideaki Miyake, Isao Hara, Soichi Arakawa, Sadao KamidonoAbstract:GRP78 induction has recently been shown to play a critical role in maintaining cell viability against several kinds of stress, including depletion of endoplasmic reticulum Ca2+ and accumulation of unglycosylated proteins, under specific experimental conditions. However, the functional significance of GRP78 induction after stressful treatment has not been well defined. This article characterizes the different biological features associated with GRP78 induction by two kinds of stress agents, Calcium Ionophore, ionomycin (IM), and glycosylation inhibitor, tunicamycin (TM), focusing on the association with apoptosis in human prostate cancer cells. Both IM and TM treatment resulted in marked induction of GRP78 transcription in androgen-dependent prostate cancer LNCaP cells maintained in medium without androgen, but not in medium containing androgen, as measured by Northern blotting and nuclear run-off assays. After pretreatment with tumor necrosis factor-α, which has potent cytotoxic effects on LNCaP cells, both IM and TM could induce substantial increases in GRP78 transcription in LNCaP cells, even in medium containing androgen. Under both experimental conditions described, DNA fragmentation assays showed a direct correlation between the onset of apoptosis in LNCaP cells after IM treatment and the initiation of GRP78 transcript induction, while induction of GRP78 expression preceded TM-induced apoptosis. To elucidate the functional differences of GRP78 induction by IM and TM, an antisense oligodeoxynucleotide (ODN) targeted against the grp78 gene was designed to reduce GRP78 expression in a sequence-specific and dose-dependent manner. Antisense GRP78 ODN treatment substantially enhanced apoptosis of LNCaP cells induced by IM compared with mismatch control ODN treatment, whereas no marked differences were observed in apoptotic features induced by TM with antisense GRP78 and mismatch control ODN treatment. Studies of additional androgen-independent prostate cancer PC3 cells also demonstrated a correlation between GRP78 induction and resistance to apoptosis after IM treatment, but not after TM treatment. These findings suggest that there are at least two GRP78 signaling pathways, which play different roles in resistance against stress-induced apoptosis. J. Cell. Biochem. 77:396–408, 2000. © 2000 Wiley-Liss, Inc.
-
Calcium Ionophore ionomycin inhibits growth of human bladder cancer cells both in vitro and in vivo with alteration of bcl 2 and bax expression levels
The Journal of Urology, 1999Co-Authors: Hideaki Miyake, Isao Hara, Kazuki Yamanaka, Soichi Arakawa, Sadao KamidonoAbstract:AbstractPurpose: The objective of this study was to characterize the antiproliferative effects of the Calcium Ionophore, ionomycin on the human bladder cancer cell line HT1376 both in vitro and in ...
